Search

Your search keyword '"Hazan-Halevy, Inbal"' showing total 194 results
Start Over Author "Hazan-Halevy, Inbal"
194 results on '"Hazan-Halevy, Inbal"'

5. Contributors

Author

Alameh, Mohamad-Gabriel, primary, Alcantara, Marice, additional, Alluin, Jessica, additional, Amero, Paola, additional, Arechavala-Gomeza, Virginia, additional, Calin, George A., additional, Corey, David R., additional, Cramer, Hagen, additional, Dammes, Niels, additional, Drolet, Daniel W., additional, Frederiksen, James, additional, Gelinas, Amy D., additional, Habib, Nagy A., additional, Hazan-Halevy, Inbal, additional, Holm, Kevin, additional, Janjic, Nebojsa, additional, Johnson, Krystal C., additional, Johnson, Samantha T., additional, Kon, Edo, additional, Kortylewski, Marcin, additional, Landesman-Milo, Dalit, additional, Lemaitre, Marc M., additional, Lincoln, Christopher, additional, Lopez-Berestein, Gabriel, additional, Lynch, Sean A., additional, Oncul, Selin, additional, Ostroff, Rachel M., additional, Peer, Dan, additional, Rodriguez-Aguayo, Cristian, additional, Rohloff, John C., additional, Rossi, Daniel, additional, Rossi, John J., additional, Rupp, Thomas M., additional, Schneider, Daniel J., additional, Soblechero-Martín, Patricia, additional, Song, Min-Sun, additional, Sood, Anil K., additional, Su, Yu-Lin, additional, Sullenger, Bruce A., additional, Voutila, Jon, additional, Weissman, Drew, additional, Williams, Preston, additional, Yu, Chunsong, additional, Yu, Haixiang, additional, Zhang, Zhuoran, additional, and Zhou, Jiehua, additional

Published
2022
Full Text
View/download PDF

6. STAT3-Activated GM-CSFRα Translocates to the Nucleus and Protects CLL Cells from Apoptosis

Author

Li, Ping, Harris, David, Liu, Zhiming, Rozovski, Uri, Ferrajoli, Alessandra, Wang, Yongtao, Bueso-Ramos, Carlos, Hazan-Halevy, Inbal, Grgurevic, Srdana, Wierda, William, Burger, Jan, O'Brien, Susan, Faderl, Stefan, Keating, Michael, and Estrov, Zeev

Subjects
Biochemistry and Cell Biology, Biological Sciences, Lymphoma, Rare Diseases, Cancer, Hematology, Genetics, Aetiology, 2.1 Biological and endogenous factors, Apoptosis, Cell Survival, Humans, Leukemia, Lymphocytic, Chronic, B-Cell, NF-kappa B, Promoter Regions, Genetic, RNA, Small Interfering, Receptors, Granulocyte-Macrophage Colony-Stimulating Factor, STAT3 Transcription Factor, Signal Transduction, Translocation, Genetic, Oncology and Carcinogenesis, Developmental Biology, Oncology & Carcinogenesis, Biochemistry and cell biology, Oncology and carcinogenesis
Abstract

UnlabelledHere, it was determined that chronic lymphocytic leukemia (CLL) cells express the α subunit, but not the β subunit, of the granulocyte-macrophage colony-stimulating factor receptor (GM-CSFR/CSF2R). GM-CSFRα was detected on the surface, in the cytosol, and in the nucleus of CLL cells via confocal microscopy, cell fractionation, and GM-CSFRα antibody epitope mapping. Because STAT3 is frequently activated in CLL and the GM-CSFRα promoter harbors putative STAT3 consensus binding sites, MM1 cells were transfected with truncated forms of the GM-CSFRα promoter, then stimulated with IL6 to activate STAT3 and to identify STAT3-binding sites. Chromatin immunoprecipitation (ChIP) and an electoromobility shift assay (EMSA) confirmed STAT3 occupancy to those promoter regions in both IL6-stimulated MM1 and CLL cells. Transfection of MM1 cells with STAT3-siRNA or CLL cells with STAT3-shRNA significantly downregulated GM-CSFRα mRNA and protein levels. RNA transcripts, involved in regulating cell survival pathways, and the proteins KAP1 (TRIM28) and ISG15 coimmunoprecipitated with GM-CSFRα. GM-CSFRα-bound KAP1 enhanced the transcriptional activity of STAT3, whereas GM-CSFRα-bound ISG15 inhibited the NF-κB pathway. Nevertheless, overexpression of GM-CSFRα protected MM1 cells from dexamethasone-induced apoptosis, and GM-CSFRα knockdown induced apoptosis in CLL cells, suggesting that GM-CSFRα provides a ligand-independent survival advantage.ImplicationsConstitutively, activation of STAT3 induces the expression of GM-CSFRα that protects CLL cells from apoptosis, suggesting that inhibition of STAT3 or GM-CSFRα may benefit patients with CLL.

Published
2014

9. Delivery of Therapeutic RNA to the Bone Marrow in Multiple Myeloma Using CD38‐Targeted Lipid Nanoparticles (Adv. Sci. 21/2023)

Author

Tarab‐Ravski, Dana, primary, Hazan‐Halevy, Inbal, additional, Goldsmith, Meir, additional, Stotsky‐Oterin, Lior, additional, Breier, Dor, additional, Naidu, Gonna Somu, additional, Aitha, Anjaiah, additional, Diesendruck, Yael, additional, Ng, Brandon D., additional, Barsheshet, Hagit, additional, Berger, Tamar, additional, Vaxman, Iuliana, additional, Raanani, Pia, additional, and Peer, Dan, additional

Published
2023
Full Text
View/download PDF

14. A modular platform for targeted RNAi therapeutics

Author

Kedmi, Ranit, Veiga, Nuphar, Ramishetti, Srinivas, Goldsmith, Meir, Rosenblum, Daniel, Dammes, Niels, Hazan-Halevy, Inbal, Nahary, Limor, Leviatan-Ben-Arye, Shani, Harlev, Michael, Behlke, Mark, Benhar, Itai, Lieberman, Judy, and Peer, Dan

Published
2018
Full Text
View/download PDF

15. A single-dose F1-based mRNA-LNP vaccine provides protection against the lethal plague bacterium

Author

Kon, Edo, primary, Levy, Yinon, additional, Elia, Uri, additional, Cohen, Hila, additional, Hazan-Halevy, Inbal, additional, Aftalion, Moshe, additional, Ezra, Assaf, additional, Bar-Haim, Erez, additional, Naidu, Gonna Somu, additional, Diesendruck, Yael, additional, Rotem, Shahar, additional, Ad-El, Nitay, additional, Goldsmith, Meir, additional, Mamroud, Emanuelle, additional, Peer, Dan, additional, and Cohen, Ofer, additional

Published
2023
Full Text
View/download PDF

19. An Effective mRNA-LNP Vaccine Against the Lethal Plague Bacterium

Author

Kon, Edo, primary, Levy, Yinon, additional, Elia, Uri, additional, Cohen, Hila, additional, Hazan-Halevy, Inbal, additional, Aftalion, Moshe, additional, Ezra, Assaf, additional, Bar-Haim, Erez, additional, Naidu, Gonna Somu, additional, Diesendruck, Yael, additional, Rotem, Shahar, additional, Ad-El, Nitay, additional, Goldsmith, Meir, additional, Mamroud, Emanuelle, additional, Peer, Dan, additional, and Cohen, Ofer, additional

Published
2022
Full Text
View/download PDF

25. Bioinspired artificial exosomes based on lipid nanoparticles carrying let-7b-5p promote angiogenesis in vitro and in vivo

Author

Aday, Sezin, primary, Hazan-Halevy, Inbal, additional, Chamorro-Jorganes, Aranzazu, additional, Anwar, Maryam, additional, Goldsmith, Meir, additional, Beazley-Long, Nicholas, additional, Sahoo, Susmita, additional, Dogra, Navneet, additional, Sweaad, Walid, additional, Catapano, Francesco, additional, Ozaki-Tan, Sho, additional, Angelini, Gianni D., additional, Madeddu, Paolo, additional, Benest, Andrew V., additional, Peer, Dan, additional, and Emanueli, Costanza, additional

Published
2021
Full Text
View/download PDF

34. Advanced Strategies in Immune Modulation of Cancer Using Lipid-Based Nanoparticles

Author

Mizrahy, Shoshy, Hazan-Halevy, Inbal, Landesman-Milo, Dalit, Ng, Brandon D., and Peer, Dan

Subjects
siRNA therapeutic, cancer immunotherapy, Immunology, tumor microenvironment, lipid nanoparticles, cancer vaccines
Abstract

Immunotherapy has a great potential in advancing cancer treatment, especially in light of recent discoveries and therapeutic interventions that lead to complete response in specific subgroups of melanoma patients. By using the body’s own immune system, it is possible not only to specifically target and eliminate cancer cells while leaving healthy cells unharmed but also to elicit long-term protective response. Despite the promise, current immunotherapy is limited and fails in addressing all tumor types. This is probably due to the fact that a single treatment strategy is not sufficient in overcoming the complex antitumor immunity. The use of nanoparticle-based system for immunotherapy is a promising strategy that can simultaneously target multiple pathways with the same kinetics to enhance antitumor response. Here, we will highlight the recent advances in the field of cancer immunotherapy that utilize lipid-based nanoparticles as delivery vehicles and address the ongoing challenges and potential opportunities.

Published
2017
Full Text
View/download PDF

37. Harnessing RNAi-based nanomedicines for therapeutic gene silencing in B-cell malignancies

Author

Weinstein, Shiri, primary, Toker, Itai A., additional, Emmanuel, Rafi, additional, Ramishetti, Srinivas, additional, Hazan-Halevy, Inbal, additional, Rosenblum, Daniel, additional, Goldsmith, Meir, additional, Abraham, Avigdor, additional, Benjamini, Ohad, additional, Bairey, Osnat, additional, Raanani, Pia, additional, Nagler, Arnon, additional, Lieberman, Judy, additional, and Peer, Dan, additional

Published
2015
Full Text
View/download PDF

39. The Cytokine Midkine and its Receptor RPTPζ Regulate B Cell Survival in a Pathway Induced by CD741

Author

Cohen, Sivan, Shoshana, Or-yam, Zelman-Toister, Einat, Maharshak, Nitsan, Ehrenreich, Inbal Binsky, Gordin, Maya, Hazan-Halevy, Inbal, Herishanu, Yair, Shvidel, Lev, Haran, Michal, Leng, Lin, Bucala, Richard, Harroch, Sheila, and Shachar, Idit

Subjects
Mice, Knockout, B-Lymphocytes, Membrane Glycoproteins, Cell Survival, Midkine, Histocompatibility Antigens Class II, Receptor-Like Protein Tyrosine Phosphatases, Class 2, Proto-Oncogene Proteins c-met, Article, Antigens, Differentiation, B-Lymphocyte, Mice, Gene Expression Regulation, Cell Line, Tumor, Animals, Cytokines, Receptors, Growth Factor, Spleen, Signal Transduction
Abstract

Lasting B cell persistence depends on survival signals that are transduced by cell surface receptors. In this study, we describe a novel biological mechanism essential for survival and homeostasis of normal peripheral mature B cells and chronic lymphocytic leukemia cells, regulated by the heparin-binding cytokine, midkine (MK), and its proteoglycan receptor, the receptor-type tyrosine phosphatase ζ (RPTPζ). We demonstrate that MK initiates a signaling cascade leading to B cell survival by binding to RPTPζ. In mice lacking PTPRZ, the proportion and number of the mature B cell population are reduced. Our results emphasize a unique and critical function for MK signaling in the previously described MIF/CD74-induced survival pathway. Stimulation of CD74 with MIF leads to c-Met activation, resulting in elevation of MK expression in both normal mouse splenic B and chronic lymphocytic leukemia cells. Our results indicate that MK and RPTPζ are important regulators of the B cell repertoire. These findings could pave the way toward understanding the mechanisms shaping B cell survival and suggest novel therapeutic strategies based on the blockade of the MK/RPTPζ-dependent survival pathway.

Published
2011

40. Signal Transducer and Activator of Transcription (STAT)-3 Activates Nuclear Factor (NF)-κB in Chronic Lymphocytic Leukemia Cells

Author

Liu, Zhiming, Hazan-Halevy, Inbal, Harris, David M., Li, Ping, Ferrajoli, Alessandra, Faderl, Stefan, Keating, Michael J., and Estrov, Zeev

Subjects
Aged, 80 and over, Cell Nucleus, Male, STAT3 Transcription Factor, Transcriptional Activation, Gene Expression Regulation, Leukemic, Transcription Factor RelA, NF-kappa B p50 Subunit, Middle Aged, Leukemia, Lymphocytic, Chronic, B-Cell, Article, immune system diseases, hemic and lymphatic diseases, Humans, Female, Phosphorylation, Cells, Cultured, Aged
Abstract

Nuclear factor (NF)-κB plays a major role in the pathogenesis of B-cell neoplasms. A broad array of mostly extracellular stimuli has been reported to activate NF-κB, to various degrees, in chronic lymphocytic leukemia (CLL) cells. Because CLL cells harbor high levels of unphosphorylated (U) signal transducer and activator of transcription (STAT)-3 protein and U-STAT3 was reported to activate NF-κB, we sought to determine whether U-STAT3 activates NF-κB in CLL. Using the electrophoretic mobility shift assay (EMSA) we studied peripheral blood low-density cells from 15 patients with CLL and found that CLL cell nuclear extracts from all the samples bound to an NF-κB DNA probe, suggesting that NF-κB is constitutively activated in CLL. Immunoprecipitation studies showed that STAT3 bound NF-κB p65, and confocal microscopy studies detected U-STAT3/NF-κB complexes in the nuclei of CLL cells, thereby confirming these findings. Furthermore, infection of CLL cells with retroviral STAT3-shRNA attenuated the binding of NF-κB to DNA, as assessed by EMSA, and downregulated mRNA levels of NF-κB-regulated genes, as assessed by quantitative polymerase chain reaction. Taken together, our data suggest that U-STAT3 binds to the NF-κB p50/p65 dimers and that the U-STAT3/NF-κB complexes bind to DNA and activate NF-κB-regulated genes in CLL cells.

Published
2011

41. STAT3-induced GM-CSFRα Protects Chronic Lymphocytic Leukemia (CLL) Cells From Apoptosis

Author

Rozovski, Uri, primary, Li, Ping, additional, Harris, David, additional, Liu, Zhiming, additional, Ferrajoli, Alessandra, additional, Bueso-Ramos, Carlos, additional, Hazan-Halevy, Inbal, additional, Grgurevic, Srdana, additional, Wierda, William, additional, Burger, Jan, additional, O’Brien, Susan, additional, Faderl, Stefan, additional, Keating, Michael, additional, and Estrov, Zeev, additional

Published
2014
Full Text
View/download PDF

42. Stimulation of the B-cell receptor activates the JAK2/STAT3 signaling pathway in chronic lymphocytic leukemia cells

Author

Rozovski, Uri, primary, Wu, Ji Yuan, additional, Harris, David M., additional, Liu, Zhiming, additional, Li, Ping, additional, Hazan-Halevy, Inbal, additional, Ferrajoli, Alessandra, additional, Burger, Jan A., additional, O’Brien, Susan, additional, Jain, Nitin, additional, Verstovsek, Srdan, additional, Wierda, William G., additional, Keating, Michael J., additional, and Estrov, Zeev, additional

Published
2014
Full Text
View/download PDF

43. STAT3-Activated GM-CSFRα Shuttles To The Nucleus and Protects CLL Cells From Apoptosis

Author

Li, Ping, primary, Rozovski, Uri, additional, Harris, David, additional, Zhiming, Lui, additional, Ferrajoli, Alessandra, additional, Bueso-Ramos, Carlos E., additional, Hazan-Halevy, Inbal, additional, Grugurevic, Srdana, additional, Wierda, William G., additional, Burger, Jan A., additional, O'Brien, Susan, additional, Faderl, Stefan H., additional, Keating, Michael J., additional, and Estrov, Zeev, additional

Published
2013
Full Text
View/download PDF

44. CD84 is a survival receptor for chronic lymphocytic leukemia cells (P2044)

Author

Marom, Ayelet, primary, Binsky-Ehrenreich, Inbal, additional, Sobotta, Mirko, additional, Shvidel, Lev, additional, Berrebi, Alain, additional, Hazan-Halevy, Inbal, additional, Kay, Sigi, additional, Aloshin, Anna, additional, Sagi, Irit, additional, Goldenberg, David, additional, Leng, Lin, additional, Bucala, Richard, additional, Herishanu, Yair, additional, Haran, Michal, additional, and Shachar, Idit, additional

Published
2013
Full Text
View/download PDF

45. Divergence in CD19-Mediated Signaling Unfolds Intraclonal Diversity in Chronic Lymphocytic Leukemia, Which Correlates with Disease Progression

Author

Herishanu, Yair, primary, Kay, Sigi, additional, Dezorella, Nili, additional, Baron, Shoshana, additional, Hazan-Halevy, Inbal, additional, Porat, Ziv, additional, Trestman, Svetlana, additional, Perry, Chava, additional, Braunstein, Rony, additional, Deutsch, Varda, additional, Polliack, Aaron, additional, Naparstek, Elizabeth, additional, and Katz, Ben-Zion, additional

Published
2013
Full Text
View/download PDF

46. Metabolism pathways in chronic lymphocytic leukemia.

Author

Rozovski, Uri, Hazan-Halevy, Inbal, Barzilai, Merav, Keating, Michael J., and Estrov, Zeev

Subjects
*CHRONIC lymphocytic leukemia treatment, *CELL metabolism, *MICRORNA, *OXIDATIVE phosphorylation, *GENETIC mutation, *LIPOPROTEIN lipase
Abstract

Alterations in chronic lymphocytic leukemia (CLL) cell metabolism have been studied by several investigators. Unlike normal B lymphocytes or other leukemia cells, CLL cells, like adipocytes, store lipids and utilize free fatty acids (FFA) to produce chemical energy. None of the recently identified mutations in CLL directly affects metabolic pathways, suggesting that genetic alterations do not directly contribute to CLL cells’ metabolic reprogramming. Conversely, recent data suggest that activation of STAT3 or downregulation of microRNA-125 levels plays a crucial role in the utilization of FFA to meet the CLL cells’ metabolic needs. STAT3, known to be constitutively activated in CLL, increases the levels of lipoprotein lipase (LPL) that mediates lipoprotein uptake and shifts the CLL cells’ metabolism towards utilization of FFA. Herein, we review the evidence for altered lipid metabolism, increased mitochondrial activity and formation of reactive oxygen species (ROS) in CLL cells, and discuss the possible therapeutic strategies to inhibit lipid metabolism pathways in patient with CLL. [ABSTRACT FROM AUTHOR]

Published
2016
Full Text
View/download PDF

48. The Cytokine Midkine and Its Receptor RPTPζ Regulate B Cell Survival in a Pathway Induced by CD74

Author

Cohen, Sivan, primary, Shoshana, Or-yam, additional, Zelman-Toister, Einat, additional, Maharshak, Nitsan, additional, Binsky-Ehrenreich, Inbal, additional, Gordin, Maya, additional, Hazan-Halevy, Inbal, additional, Herishanu, Yair, additional, Shvidel, Lev, additional, Haran, Michal, additional, Leng, Lin, additional, Bucala, Richard, additional, Harroch, Sheila, additional, and Shachar, Idit, additional

Published
2012
Full Text
View/download PDF

49. Signal Transducer and Activator of Transcription (STAT)-3 Induces Granulocyte/Macrophage Colony-Stimulating Factor (GM-CSF) Receptor-α Expression in Chronic Lymphocytic Leukemia (CLL) Cells,

Author

Li, Ping, primary, Liu, Zhiming, additional, Harris, David, additional, Ferrajoli, Alessandra, additional, Wang, Yongtao, additional, Hazan-Halevy, Inbal, additional, Grgurevic, Srdana, additional, Wierda, William G., additional, Burger, Jan A., additional, O'Brien, Susan, additional, Faderl, Stefan, additional, Keating, Michael J, additional, and Estrov, Zeev, additional

Published
2011
Full Text
View/download PDF

50. 2.7 Intra-Clonal Diversity Identified by CD19-Mediated Signaling Correlates with Disease Progression in CLL

Author

Herishanu, Yair, primary, Kay, Sigi, additional, Dezorella, Nili, additional, Baron, Shoshana, additional, Hazan-Halevy, Inbal, additional, Trestman, Svetlana, additional, Perry, Chava, additional, Braunstein, Rony, additional, Deutsch, Varda, additional, Polliack, Aaron, additional, Naparstek, Elizabeth, additional, and Katz, Ben-Zion, additional

Published
2011
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results